Lower extremity artery disease (LEAD) is a chronic inflammatory disease that occurs when atherosclerotic plaques form in the lower extremities, which may lead to amputation if not manged properly. Given clinical standardcare (pharmacological and surgical) have limited efficacy in LEAD, developing novel strategies to manage LEAD remains an unmet clinical need. Given that active resolution of inflammation is essential to facilitate tissue healing and repair, failure to resolve inflammation may lead to chronic inflammation, dysregulated cellular homeostasis and adverse tissue remodeling. Several studies have demonstrated the importance of the balance between endogenous pro-resolving mediators and pro-inflammatory factors. There is growing evidence to suggest endogenous pro-resolving mediators engage with pro-resolving G-protein-coupled receptors to reduce the initiation and progression of inflammatory responses and to increase therapeutic angiogenesis in LEAD. Here, we highlight the mechanisms and the consequences of resolved inflammation, and the therapeutic potential of endogenous pro-resolving mediators-based strategy for this devastating disease.

下肢动脉疾病（LEAD）是一种慢性炎症性疾病，发生在下肢动脉粥样硬化斑块形成时，如果处理不当可能导致截肢。鉴于临床标准治疗（药理学和外科手术）在 LEAD 中的疗效有限，开发管理 LEAD 的新策略仍然是未满足的临床需求。鉴于炎症的主动消退对于促进组织愈合和修复至关重要，未能消退炎症可能导致慢性炎症、细胞稳态失调和不利的组织重塑。一些研究已经证明了内源性促分解介质和促炎因子之间平衡的重要性。越来越多的证据表明，内源性促分解介质与促分解 G 蛋白偶联受体结合可减少炎症反应的起始和进展，并增加 LEAD 中的治疗性血管生成。在这里，我们强调了炎症消退的机制和后果，以及基于内源性促消解介质的策略对这种破坏性疾病的治疗潜力。